.1 Antisense Nucleic Acid In Vitro Anti-radiation Effect Of Two Anti-cancer Effect Of Dihydroartemisinin

In vitro anti-radiation effects of antisense thiodeoxyoligonucleotides targeted to bax mRNAObjective: It is one of importent mechanism that radiation bring out body damage for apoptosis. The decrease of the value of Bcl-2/Bax proteins is a key checkpoint of apoptotic initiation by radiation. The goal of the present study was to try increasing the value of Bcl-2/Bax proteins and further inhibiting radiation-induceed apoptosis though reducing translation of Bax protein with antisense thiodeoxyoligonucleotides targeted to bax mRNA, caspase-3-mRNA, which will be benefited for enhancing cell survival and plerosis, It will be reaserched for possiblity that antisense thiodeoxyoligonucleotides be developed into latent new type anti-radiation drugMethods: The survival profile of human embryonic lung fibroblast (HELF) and mouse CFU-GM were determined, with MTT assay, SRB assay and CFU-GM colony formation, immediately exposed to 100nmol L-1 of the drug candidate 6h after -ray radiation. With RT-PCR and flow cytometry, the alteration of bax mRNA expression and cell cycle in HELF were examined in order to explore its mechanisms.Results: The survival rate of HELF increased 24.4% (MTT) and 12.8% (SRB) (P<0.01) via treatment for TXC002. none of caspase-3 mRNA ODNs show effect. The counts of CFU-GM colonies in drug candidate-treated group significantly outweighed one in control (72 17 vs 13 6, P>0.01). The result of RT-PCR showed that the ratio between bax strip and -actin strip in drug candidate-treated group and control were 43.9% and 68.6%, respectively. The proportion of total S-phase of HELF of treated group was 24.2% and 7.7% in control in the analysis of flow cytometry. The above suggested that the copies of bax mRNA in treated cells was lower than in control cells, and having more activities of proliferation. Conclusions: The antisense thiodeoxyoligonucleotides could promote the survival of cells exposed to Y -ray, and its mechanisms might involved with reducing translation of Bax protein secondary to damaging target mRNA, inhibiting apoptotic initiation and having active proliferation.